This study adhered to MOOSE guidelines.Databases were searched for studies comparing KRAS, BRAF, microsatellite instability (MSI), CpG island methylator phenotype (CIMP), p53 and p27 status between patients with mucinous and non-mucinous colorectal adenocarcinoma.
Our data reveal the characteristic cytoplasmic sequestration of p53 by the heat shock protein mortalin in human colorectal adenocarcinoma cell lines, as is the case for other cancers, such as glioblastomas and hepatocellular carcinomas.
Expression of mutant p53 and of the multidrug resistant proteins P-glycoprotein and glutathione S-transferase-pi correlated in colorectal adenocarcinoma.
Metalloproteinase-1, metalloproteinase-7, and p53 immunoexpression and their correlation with clinicopathological prognostic factors in colorectal adenocarcinoma.
Maspin expression correlated negatively with liver metastasis of CRA (p < 0.05), positively with tenascin expression (p < 0.05), but not with tumor size, depth of invasion, local invasion via vessels, lymph node metastasis, differentiation, expression of Ki-67 and p53 or MVD (p > 0.05).
All the patients with colorectal mucinous adenocarcinoma and colorectal signet-ring cell carcinoma with a positive family history of colorectal adenocarcinoma had tumors that showed p53 expression (P = 0.012).
Multiple sample areas in colorectal adenocarcinoma at early and advanced stages and in metastases were studied for the well-known genetic alterations: K-ras and p53 point mutations and loss of heterozygosity (LOH) on chromosomes 5q and 18q.
Genetic alteration of p53, but not overexpression of intratumoral p53 protein, or serum p53 antibody is a prognostic factor in sporadic colorectal adenocarcinoma.
These results reveal that immunohistochemical assessment does not predictTP53 mutation status in colorectal adenocarcinoma, mainly in cases displaying absence of nuclear staining.
Therefore, the purpose of our study was to determine the prognostic value of BAX protein expression and the mutational status of its upstream regulator p53 in primary colorectal adenocarcinoma.
Taken together, these data imply that deregulated expression of Id proteins in colorectal adenocarcinoma arises at least in part as a consequence of loss of p53 function and contributes to the uncontrolled proliferation of tumor cells in colorectal cancer.
Archival formalin-fixed, paraffin-embedded tissues from seven cases of colorectal adenocarcinoma were laser- and hand-microdissected and subsequently evaluated by PCR/SSCP/sequencing for Ki-ras exon 1 and p53 exons 5, 7, and 8.Results.
We investigated the relationship between oral contraceptive use and other reproductive factors with p53 over-expression in 64 post-menopausal women, 45-86 years of age, with non-familial colorectal adenocarcinoma.
In contrast to colorectal adenocarcinoma, which demonstrates K-ras-2 mutation in about 50% of cases, ITAC showed no evidence of K-ras-2 mutation. p53 mutations were present in 18% of ITAC (2 of 11) compared to more than 75% incidence of p53 mutation seen in colorectal adenocarcinoma.